Neurogenic Mutism 3/25/25
Neurogenic Mutism Notes
Definition of Mutism
Mutism: Absence of speech.
Can be deliberate (mute on purpose) or a result of psychiatric disturbances.
children and adults choose to be mute (Einstein), selective in who they might converse with = selective mutism
Possible organic causes:
Profound, uncorrected congenital hearing loss.
Peripheral structural loss (e.g., laryngectomy).
can a person with MSD develop mutism?
can be organic but nonneurologic
laryngectomy can cause it too bc no larynx=no speech
aquired neurogenic mutism
Causes of Mutism
Neurogenic: Resulting from neurological conditions affecting:
Peripheral Nervous System
Central Nervous System (CNS): Affects areas from brainstem to cortex.
neurogenic mutism can take several forms, resulting from severe dysarhtrira, AOS, aphasia, etc
Types of Mutism Discussed:
Congenital Neurogenic Mutism: Not covered in this chapter.
Psychogenic Mutism: Addressed in Chapter 14.
Various forms based on underlying conditions:
Severe dysarthria
Apraxia of Speech (AOS)
Aphasia
Cognitive and affective conditions
Medical circumstances post-seizure or surgical procedures.
Anarthria
Definition: Speechlessness due to severe loss of neuromuscular control over speech. inability to produce speech. most severe form of dysarthria
Clinical Characteristics:
Intact language and cognitive abilities.
Emotional drive to communicate but physically unable to speak.
neuro damage makes it so they cannot speak
Types of Neurogenic Mutism
1. Clinical Subtypes
Spastic Dysarthria: Bilateral upper motor neuron damage; oromotor spasticity, severe dysphagia.
Flaccid Dysarthria: Lower motor neuron damage; oromotor weakness.
Hypokinetic & Hyperkinetic Dysarthria: Basal ganglia dysfunction.
Aphasia: Severe multimodality language impairment.
Coma and Vegetative State: No voluntary behavior; respond to stimuli.
Akinetic Mutism: Frontal lobe and midbrain damage; unresponsive but aware.
Etiologies of Neurogenic Mutism
ALS (Amyotrophic Lateral Sclerosis): 44% of cases result in anarthria.
Stroke: 10% - leads to anarthria and AOS.
Demyelinating Diseases: 6% - e.g., Multiple Sclerosis.
Closed Head Injury: 5% - often anarthria with cognitive deficits.
Other: Cerebral palsy, anoxia, brain tumors (16%).
Locked-In Syndrome (LiS)- slide 8
Characteristics:
Anarthria with quadriplegia; only vertical eye movements preserved.
Individual is conscious and can communicate via eye movements.
most often could be mixed spastic-flaccid or severe spastic dysarthria
person is there but they seem locked in, only thing that is voluntary is eye movement and blinking. they are usually cognitively aware and receptive is great, but they communicate with eye movements
when the etiology is brainstem stroke, there is a high risk for death in the first days to months. neuroplasticity of your brain is what matters! the younger you are, the longer you will live usually
more than 40% ability to feed orally, read=77%, communicate verbally= 28%
Prognosis:
Long-term survival is better with nonvascular causes.
Recovery of motor functions varies widely (20% may regain some functions).
Cognitive deficits can persist based on lesion location. SLIDE 10
if there has been a lesion in the pontine brain, this can negatively impact an individual, but if their cognitive skills are intact, lesion may be on brainstem
Biopercular Syndrome- slide 11
varying degrees of dysarthria, including mutism
caused by bilateral damage to the lower part of the precentral and postcentral gyri of the cerebral hemisphere
Characterized by:
Severe orofacial mobility deficits; facial weakness.= face, jaw and palatal movements are hypotonic
inability to voluntary close eyes or frown
Muteness with minimal low volume voluntary speech.
Caused by damage to the Rolandic operculum in the brain.
Cerebellar Mutism (Posterior Fossa Syndrome)- slide 13
posterior fossa= next to the foramen like the hole where brain and spinal cord connect
emerges after posterior fossa surgery due to tumor
part of cerebellum and midbrain
uncommon in adults bc PF tumors are more common in children. average age is 6-9
mutism can last up to 12 months in longer cases, depending on recovery
average duration is 4-8 weeks (transient) = good prognosis to regain speech
Primarily seen in children post-surgery for posterior fossa tumors.
Development of mutism can occur days to weeks post-surgery.
Mutism is usually transient, resolving with ataxic dysarthria following.
Apraxia and Mutism- slide 15
AOS can lead to acute mutism post-stroke.
Rarely persistent beyond initial phases.
Prolonged mutism may indicate other complications such as dysarthria or cognitive deficits.
if they have AOS, they can be mute for a long time
Case Studies Analysis
Case 1: 65-Year-Old Woman
Condition after stroke, demonstrated anarthria with significant cognitive deficits.
Communication limited to nonverbal (head nods and eye blinks).
just bc someone cannot speak, does not mean they cannot develop some form of communication!!!!! find a way they can communicate to you!
Case 2: 5-Year-Old Boy with Postoperative Mutism
Developed mutism following fourth ventricle tumor surgery; cognitive and motor abilities gradually emerged over time.
Suggestive of cerebellar mutism or AOS without clear psychogenic component.
Chapter Summary
Origins of Mutism: Varied, includes neurologic origins (acquired conditions).
Anarthric Mutism: Resulting from bilateral neurologic damage; often brainstem involvement.
Locked-In Syndrome: Characterized by mutism and quadriplegia with preserved cognition.
Associated Conditions: Various neurologic pathologies lead to different mutism types.
Acute Stroke Impact: Mutism may develop with AOS; persistence may indicate further issues.
Cognitive/Affective Factors: Distinct from motor explanations contributing to mutism.
Neurologic Events: Specific neurologic incidents can trigger mutism, highlighting need for a detailed clinical assessment.